Reperfusion failure despite recanalization in stroke: New translational evidence

Current treatment for acute ischemic stroke aims at recanalizing the occluded blood vessel to reperfuse brain tissue. Clot removal can be achieved pharmacologically with a thrombolytic drug, such as recombinant tissue plasminogen activator, or mechanical thrombectomy. However, reopening does not guarantee full reperfusion, which has been referred reperfusion failure. When it occurs, failure significantly attenuates beneficial effect of recanalization therapy and severely affects functional recovery patients. The mechanisms are somewhat complex fully understood. Briefly, after stroke, capillaries show stalls, constriction luminal narrowing, being crowded neutrophils, fibrin–platelet deposits. Furthermore, in patients, primary clot break, dislodge, occlude distal arterial branches further downstream. In this review, we highlight rodent model that allows studying pathophysiological underlying stroke. We also describe vascular intravascular changes involved may provide relevant therapeutic targets improving